Browse our anti-GNAS (GNAS) Antibodies

Full name:

anti-GNAS Complex Locus Antibodies (GNAS)

On www.antibodies-online.com are 174 GNAS Complex Locus (GNAS) Antibodies from 22 different suppliers available. Additionally we are shipping GNAS Proteins (16) and GNAS Kits (12) and many more products for this protein. A total of 218 GNAS products are currently listed.

More Antibodies against GNAS Interaction Partners

Human GNAS Complex Locus (GNAS) interaction partners

Activating GNAS (R201C) mutations were found in 2 unrelated patients with virilizing ovarian Leydig cell tumors. This mutation and subsequent cAMP increase may play a significant role in the pathogenesis of virilizing LCT through the stimulation of androgen production and tumor development.

mutation analysis of GNAS by pyrosequencing has diagnostic value in FFPE tissue of patients with FD, especially in specimens that were not decalcified. The R201H substitution mutation of GNAS may be involved in the pathogenesis of polyostotic FD.

GNAS mutations can be used as good diagnostic tool to distinguish intramuscular / cellular myxoma from low-grade myxofibrosarcoma, especially on biopsy material.

GNAS T/C 393 frequencies were similar in control and PHPT groups. No association was found between genotypes and clinical expression of PHPT. A nonstatistically significant trend was seen to lower BMD in the lumbar spine, femoral neck, and total hip in both PHPT and control C homozygote subjects. A C allele-related susceptibility to lower BMD in trabecular bone in both groups is not enough to suggest more severity.

model suggests Cys1004 in AC6 (subunit C2) and Cys174 in Galphas present at the AC-Galphas interface as the possible residues that might undergo reversible nitrosylation. Docking analysis predicted novel ligands of AC6 that include forskolin-based compounds and its derivatives.

In a cohort of patients with pancreatic cysts, KRAS and GNAS mutations had no significant diagnostic benefit in comparison with conventional testing.

High GNAS expression is associated with poor prognosis in intrahepatic cholangiocarcinoma.

we did not observe GNAS or BRAF mutations in urachal adenocarcinomas

GNAS mutation is a highly specific test for IPMN. When GNAS testing is added to CEA and KRAS, a significantly greater overall accuracy (86.2%) is achieved.

Our study demonstrates that GNAS mutations are present in a small subset (0.8%) of primary lung carcinomas.

Mutation in GNAS is associated with Albright Hereditary Osteodystrophy.

Both tissue blocks examined were positive for a GNAS p.R201H (c.602G>A) mutation (Fig. 3) at an allele frequency of 4.3 and 9.6%

We now describe a family in which the female proband and her daughter with a maternally inherited 2015-bp deletion that includes GNAS exon 1

An association of the GNAS1 T393C polymorphisms with risk of aseptic loosening after total hip arthroplasty is unlikely.

GIV is a bifunctional modulator of G proteins; it serves as a guanine nucleotide dissociation inhibitor (GDI) for Galphas using the same motif that allows it to serve as a guanine-nucleotide exchange factor for Galphai

GNAS harbors 2 SNPs that were associated with an increased risk for ventricular tachyarrhythmia in implantable cardioverter defibrillator patients, of which 1 was successfully replicated in a community-based population of sudden cardiac death cases.

RAS and GNAS mutations were associated with worse progression-free survival (PFS) at univariate analysis (P = 0.006 and 0.011, respectively). At multivariate analysis, only KRAS mutations were independently associated with PFS (P = 0.012); GNAS mutations were not-being significantly associated with other poor prognostic features such as incomplete cytoreduction or KRAS mutations

Pig (Porcine) GNAS Complex Locus (GNAS) interaction partners

The Galphas and Galphaq peptides adopt different orientations in beta2-AR and V1AR, respectively. The beta2-AR/Galphas peptide interface is dominated by electrostatic interactions, whereas the V1AR/Galphaq peptide interactions are predominantly hydrophobic.

Target RNA interference of GNAS in porcine fibroblast cells leads to lower mRNA expression of Bcl-2, Fas, and Caspase-3, which are recognized as apoptosis related markers.

Imprinting analysis showed that NESP55 is maternally expressed in young and adult pigs.

meiotic resumption of porcine oocytes is prevented by ooplasmic Gsalpha, which may stimulate cAMP synthesis within porcine oocytes

Review article on the human GNAS complex locus.

Mouse (Murine) GNAS Complex Locus (GNAS) interaction partners

In mice that express activated KRAS in the pancreas, we found expression of GNAS(R201C) to cause development of more differentiated tumors, with gene expression pattern associated with the ductal phenotype.

This study presents an unexpected proinflammatory switch from Galphas to GalphaI glp1r signaling in burn monocytes which promotes ERK1/2 and NF-kappaB activation

This study demonstrates that induced expression of the fibrous dysplasia (FD) Galphas mutant from the mouse endogenous Gnas locus exhibits human FD phenotypes in vivo, and that inhibitors of Wnt/beta-catenin signaling may be repurposed for treating FD and other bone diseases caused by Galphas activation.

high osteoblastic GalphaS expression results in aberrant skeletal development in which bone production is favored at the cost of bone quality.

Our findings suggest that a cis-acting factor could be implicated in reducing paternal Galphas expression in brown adipose tissue

Our data revealed a positive correlation between hepatic Gsalpha-cAMP signal axis and fasting blood glucose (FBG) in slight insulin resistance stage of HIgh Sugar High Fat-diet rats and diabetic db/db mice. The current finding thus suggested hepatic Gsalpha-cAMP signal axis plays a central role in regulating of FBG during the developing and development of T2DM.

in colonic crypt cultures, the GLP-1 secretion induced by such Gq + Gs GPR40 agonists is indeed inhibited by blockers of both Gq and Gs and is eliminated by combining these.

retrograde trafficking to the trans-Golgi network induces local Gs-protein activation and cAMP/PKA signaling at a critical position near the nucleus, which appears required for efficient CREB phosphorylation and gene transcription

Gsalpha deficiency in JG cells of adult mice results in kidney injury, suggesting that JG cells are critically involved in the maintenance and protection of the renal microvascular endothelium.

results show that most of the PatDp(dist2) phenotype is due to overexpression of Gnasxl combined with loss of expression of Gnas, and suggest that Gnasxl and Gnas may act antagonistically in a number of tissues and to cause a wide range of phenotypic effects

results show that Gsalpha imprinting in the dorsomedial nucleus of the hypothalamus (DMH) underlies the parent-of-origin metabolic phenotype that results from Gsalpha mutations and that DMH MC4R/Gsalpha signaling is important for regulation of energy expenditure and brown adipose tissue activation, but not the metabolic response to cold.

Authors demonstrated that Nesp55 is co-localized with serotonin and then went on to show that in midbrain regions there were reductions in mRNA expression of the serotonin-specific genes Tph2 and Slc6a4, but not the dopamine-specific gene Th in Nesp(m/+) mice.

Disruption of Gnas in smooth muscle of mice reduced intestinal motility and led to death within 4 weeks. GNAS disruption in adults impaired contraction of intestinal smooth muscle and peristalsis with features of intestinal pseudo-obstruction characterized by chronic intestinal dilation and dysmotility.

The Galphas and Galphaq peptides adopt different orientations in beta2-AR and V1AR, respectively. The beta2-AR/Galphas peptide interface is dominated by electrostatic interactions, whereas the V1AR/Galphaq peptide interactions are predominantly hydrophobic.

the results presented here indicate an important role for the imprinted GNAS cluster in underlying complex

maternally expressed like its counterparts in mouse and human

a nucleotide-free state of Galphas is induced by Cu2+ and Zn2+

GNAS Antigen Profile

Antigen Summary

This locus has a highly complex imprinted expression pattern. It gives rise to maternally, paternally, and biallelically expressed transcripts that are derived from four alternative promoters and 5' exons. Some transcripts contain a differentially methylated region (DMR) at their 5' exons, and this DMR is commonly found in imprinted genes and correlates with transcript expression. An antisense transcript is produced from an overlapping locus on the opposite strand. One of the transcripts produced from this locus, and the antisense transcript, are paternally expressed noncoding RNAs, and may regulate imprinting in this region. In addition, one of the transcripts contains a second overlapping ORF, which encodes a structurally unrelated protein - Alex. Alternative splicing of downstream exons is also observed, which results in different forms of the stimulatory G-protein alpha subunit, a key element of the classical signal transduction pathway linking receptor-ligand interactions with the activation of adenylyl cyclase and a variety of cellular reponses. Multiple transcript variants encoding different isoforms have been found for this gene. Mutations in this gene result in pseudohypoparathyroidism type 1a, pseudohypoparathyroidism type 1b, Albright hereditary osteodystrophy, pseudopseudohypoparathyroidism, McCune-Albright syndrome, progressive osseus heteroplasia, polyostotic fibrous dysplasia of bone, and some pituitary tumors.